Editing Reactive oxygen species (section)

===Carcinogenesis===
ROS-related oxidation of DNA is one of the main causes of mutations, which can produce several types of DNA damage, including non-bulky (8-oxoguanine and formamidopyrimidine) and bulky (cyclopurine and etheno adducts) base modifications, abasic sites, non-conventional single-strand breaks, protein-DNA adducts, and intra/interstrand DNA crosslinks.<ref>{{Cite journal |vauthors=Waris G, Ahsan H |date=May 2006 |title=Reactive oxygen species: role in the development of cancer and various chronic conditions |journal=Journal of Carcinogenesis |volume=5 |pages=14 |doi=10.1186/1477-3163-5-14 |pmc=1479806 |pmid=16689993 |doi-access=free}}</ref> It has been estimated that endogenous ROS produced via normal cell metabolism modify approximately 20,000 bases of DNA per day in a single cell. 8-oxoguanine is the most abundant among various oxidized nitrogeneous bases observed. During DNA replication, DNA polymerase mispairs 8-oxoguanine with adenine, leading to a G→T transversion mutation. The resulting genomic instability directly contributes to carcinogenesis. Cellular transformation leads to cancer and interaction of atypical PKC-ζ isoform with p47phox controls ROS production and transformation from apoptotic cancer stem cells through [[blebbishield emergency program]].<ref>{{Cite journal |vauthors=Jinesh GG, Taoka R, Zhang Q, Gorantla S, Kamat AM |date=April 2016 |title=Novel PKC-ζ to p47 phox interaction is necessary for transformation from blebbishields |journal=Scientific Reports |volume=6 |pages=23965 |bibcode=2016NatSR...623965J |doi=10.1038/srep23965 |pmc=4819220 |pmid=27040869}}</ref><ref>Jinesh GG, Kamat AM. [http://www.nature.com/cdd/journal/vaop/ncurrent/full/cdd201626a.html Blebbishield emergency program: an apoptotic route to cellular transformation]. Cell Death Differ. 2016 In Press.</ref>